ABSTRACT
Refractory status epilepticus is commonly defined as status epilepticus that fails to respond to two or more appropriately dosed intravenous anti-seizure medications including at least one non-benzodiazepine drug. Super-refractory status epilepticus (SRSE) is when status epilepticus continues for ≥24 h despite anesthetic treatment or recurs on an attempted wean of the anesthetic drugs. There is little evidence to guide the management of SRSE. Of late, unconventional therapies have been described in the literature regarding the management of SRSE, with ketamine leading the pack. Studies have noted ketamine's therapeutic efficacy up to 91% in SRSE cessation. Common side effects of ketamine include nausea, vomiting, headache, and hallucinations; but to our knowledge, ketamine has not been implicated in the pathogenesis of abdominal compartment syndrome. We describe a 74-year-old male who developed severe abdominal compartment syndrome in the setting of ketamine infusion for new-onset SRSE to increase awareness about this potential complication.
ABSTRACT
BACKGROUND: Increasing evidence shows that inflammation plays an important role in the occurrence and progression of acute ischemic stroke. The receptor for advanced glycation end products (RAGE) has been documented to involve in the pathogenic mechanisms of a variety of neurological diseases, including ischemic stroke (IS). However, the impact of RAGE gene polymorphisms on the susceptibility to IS has not been reported. We thus explored the association between RAGE gene polymorphisms and the susceptibility to IS. METHOD: A total of 384 patients with IS and 425 healthy controls were enrolled in this study. Three genetic polymorphisms of RAGE gene (82G/S, -429T/C and -374T/A) were determined. The serum levels of soluble RAGE (sRAGE), intetleukin-6 (IL-6), high sensitivity-C reaction protein (hs-CRP) and plasminogen activator inhibitor-1 (PAI-1) were detected. RESULTS: Among the studied polymorphisms, only the polymorphism at 82G/S of RAGE gene was associated with the risk for ischemic stroke irrespective of the stroke subtypes. The 82S/S homozygote carriers had a significantly increased risk for ischemic stroke [adjusted odds ratio (OR): 2.297; p<0.001]. The haplotype analyses showed that the C-429S82T-374 and T-429S82A-374 had higher risk to develop IS (OR=1.864 and 1.931, respectively, all p<0.01), while the C-429G82T-374 showed a protective effect against IS susceptibility (OR=0.568, p=0.001). In addition, the 82S/S homozygote carriers had a higher inflammatory level compared with 82G/S and 82G/G genotypes, indicated by lower serum sRAGE level, higher serum IL-6, hs-CRP and PAI-1 levels. The polymorphisms at -374 and -429 loci did not influence the stroke risk and the above mentioned inflammation cytokines. CONCLUSION: Our results showed a close correlation between the 82G/S polymorphism and the susceptibility to IS, suggesting the 82G/S polymorphism may be used as a genetic marker for the prediction of stroke occurrence in high risk subjects.
